Type 2 diabetes is an epidemic disease strongly associated with obesity. The relationship between both disorders is of such interdependence that the term 'diabesity' has been coined. Although the lung is not considered a target organ in type 2 diabetes, increasing evidence through cross-sectional studies has appeared showing the opposite. In fact, diabetes is frequently co-morbid with chronic obstructive pulmonary disease, and data from the Atherosclerosis Risk in Communities Study showed a faster pulmonary function decline in type 2 diabetic patients than in other participants. This is undeniably significant, because airflow limitation is an independent predictor of death in type 2 diabetes. The available data suggest that the appearance of structural changes in respiratory muscle associated with insulin resistance, non-enzymatic glycosylation of the connective tissue, defects in the stimulation of pulmonary surfactant production and the presence of a low-grade chronic inflammation state should be considered among the possible mechanisms involved in this relationship. In addition, we have recently shown that: [i] T2DM adversely affects breathing during sleep, becoming an independent risk factor for severe nocturnal hypoxemia in obese patients; [ii] the presence of diabetes and the degree of glycaemic control are related to respiratory function impairment in morbidly obese women. Therefore, the impact of type 2 diabetes on pulmonary function should be taken into consideration by those providing care for obese people. Finally, insulin resistance was also related to respiratory function impairment in morbidly obese women, suggesting that the metabolic pathways related to insulin resistance are crucial in initiating lung abnormalities described in type 2 diabetic patients. © 2012 Nova Science Publishers, Inc. All rights reserved.
|Title of host publication||Respiratory Diseases: Causes, Treatment and Prevention|
|Number of pages||10|
|Publication status||Published - 1 Jan 2012|